Immunologic functions are mediated by two developmentally independent, but functionally interacting, families of lymphocytes. The activities of B and T lymphocytes and their products in host defense are closely integrated with the functions of other cells of the reticuloendothelial systems, such as macrophages and polymorphonuclear leukocytes, as well as with basophils and tissue mast cells.
Immunodeficiency syndromes, whether congenital, spontaneously acquired, or iatrogenic, are characterized by unusual susceptibility to infections and, sometimes, to autoimmune disease and to lymphoreticular malignancies. The types of infection often provide the first clue to the nature of the immunologic defect.
Patients with defects of humoral immunity have recurrent or chronic sinopulmonary infection, meningitis, and bacteremia, most commonly caused by pyrogenic bacteria such as Hemophilus influenzae, Streptococcus pneumoniae, and Staphylococci. Lawton, A. R., et al., Immune Deficiency Diseases, in Petersdorf, R. G., et al., eds., Harrison's Principles of Internal Medicine, 10th ed., 1983, p. 354.
Abnormalities of cell-mediated immunity predispose to disseminated viral infections, particularly with latent viruses such as herpes, varicella zoster, and cytomegalo-virus. Patients so affected also almost invariably develop mucocutaneous conditions, and frequently acquire widely disseminated fungal infections. Id at 355.
The most severe form of immune deficiency occurs in individuals, often infants, who lack both humoral and cell-mediated immune functions. They are susceptible to the whole range of infectious agents, including organisms not ordinary considered pathogenic. Multiple infections with viruses, bacteria, fungi and protozoa occur, often simultaneously.
Cryptosporidiosis, which has been seen in patients with human immunodeficiency virus and acquired immune deficiency syndrome (HIV/AIDS), is caused by the coccidian protozoa parasite, Cryptosporidium. This human pathogen is associated with severe enteritis and, perhaps, cholecystitis in immunocompromised patients, particularly those with HIV/AIDS. The same organism is also associated with significant, although self-limited, diarrheal illness in the immunocompetent host. The number of reported cases of cryptosporidiosis is continually increasing since it was first described in 1976, as more physicians become aware of the disease and microbiologists learn to identify the parasite Soave, R. et al., Controversies in the Diagnosis and Management of Infectious Diseases, 1986, pp. 1012-1022. Cryptosporidia appear to invade the microvillus border of gastrointestinal epithelial cells, and have been implicated in enteritis in animals as well as in humans.
The organism is capable of crossing species barriers. Indeed, it has been reported that immunocompetent persons who have been in contact with the feces of Cryptosporidia-infected farm animals with diarrhea, may themselves become infected with this protozoan parasite, and may present with the classical symptoms of malaise, nausea, headache, abdominal cramps, and diarrhea. Current, W. L., et al., New England Journal of Medicine 308:1252-1257 (1983).
Instances of person-to-person transmission of symptomatic infection have also been reported, occurring in both the community and hospital settings. Wetherbee, supra, at 680.
In patients with or without risk for HIV/AIDS, cryptosporidiosis occurs with a severity and duration apparently proportional to the degree of immunocompromise in the patient. Symptoms of cryptosporidiosis include abdominal pain, nausea, vomiting, and intermittent watery diarrhea without blood or mucus. Fever may or may not be present, but weight loss is significant in most cases. Diagnosis of cryptosporidiosis may often be missed. For example, the chronic diarrhea, prolonged fever, extreme weight loss, anorexia, and severe infection, in a group of HIV/AIDS patients, was referred to as “unexplained.” Malebranche, R. et al., Lancet 873-877 (Oct. 15, 1983). It is likely that these symptoms were due to undiagnosed cryptosporidiosis. Diagnosis of cryptosporidiosis is achieved through identification of Cryptosporidia oocysts in the stool, as the spherical organisms are sloughed off from the intestinal atrophic microvillus border tissue.
The currently advised therapy for cryptosporidial infection is treatment with nitazoxanide. However, it is only approved and indicated for use in immunocompetent patients. Although the immunocompetent host usually has a self-limited illness, there have been reports of severe enteritis requiring hospitalization of these patients. Efficacious anti-cryptosporidial therapy could be useful in decreasing morbidity as well as the length of time oocyst shedding occurs in the immunocompetent host infected with Cryptosporidia. In the immunocompromised patient, such as those suffering with HIV/AIDS, cryptosporidiosis is usually persistent, and causes significant malnutrition and morbidity. Current treatment is limited to symptomatic support through parenteral fluid, electrolyte, trace element, and nutrition repletion, as well as administration of anti-secretory and anti-peristaltic pharmaceuticals, or anti-parasitic or antiretroviral therapies.
For the immunocompromised host, the need for efficacious therapy is more pronounced than for the immunocompetent individual. A vast array of antimicrobial, immunomodulatory and nonspecific anti-diarrheal drugs, as well as special diets, have been administered to such patients. With few exceptions, attempts at therapeutic intervention have met with failure, both in the control of enteric symptoms and in the eradication of the parasite. Soave et al, supra, at 1012.
An important need exists, therefore, for an effective method for both preventing and treating disorders due to parasitic protozoa such as Cryptosporidia. 
Isospora belli, a related parasitic protozoa, can cause a similar syndrome in patients with HIV/AIDS; an incidence of 15% in HIV/AIDS patients has been reported. DeHovitz et al., New England Journal of Medicine, 315:87-90 (1986). Although isosporiasis responds to therapy with trimethoprim-sulfamethoxazole, it is associated with an extremely high rate of recurrence.
It has been known in the prior art to produce milk having a variety of therapeutic effects. Beck, for example, has disclosed a milk containing antibody to Streptococcus mutans which has a dental caries inhibiting effect (Beck, U.S. Pat. No. 4,324,782). The milk is obtained by hyper-immunizing a cow with Streptococcus mutans antigen and obtaining the therapeutic milk therefrom. Beck has also described a milk having anti-arthritic properties (U.S. application Ser. No. 875,140, filed Feb. 6, 1978) and has described and patented a milk having anti-inflammatory properties (U.S. Pat. No. 4,284,623). Heinbach (U.S. Pat. No. 3,128,230), has described and patented a cow milk having alpha, beta, and gamma globulins against antigenic haptens. Singh (U.S. Pat. No. 3,911,108), Peterson (U.S. Pat. No. 3,376,198 and Canadian Pat. No. 587,849), Holm (U.S. application (published) Ser. No. 628,987), and Tunnak et al. (Great Britain Patent No. 1,211,876), have also described antibody-containing milks. (U.S. Pat. No. 5,106,618).
None of these aforementioned references, however, disclose or suggest milk having anti-infective properties against gastrointestinal microbial pathogens.